Chronic tubular obstruction may activate a single nephron tubular-glomerular feedback mechanism which acts to reduce glomerular blood flow and glomerular capillary hydrostatic pressure in the obstructed nephron. Such a mechanism would shift blood flow away from a blocked nephron and might lead to atrophy of the affected nephron. The objective of the proposed research is to examine critically the proposed glomerular-tubular feedback mechanism. Single tubules in the frog and rat kidney will be obstructed by microinjection of caster oil or solid paraffin. In the frog kidney, glomerular capillary pressure after one or two days of obstruction will be measured with a servo-null pressure measuring system by glomerular puncture. Tubules in the frog kidney will also be made chronically leaky, and the effects on glomerular pressure studied. In the rat kidney, stop-flow pressures in response to chronic (24 hr) blockage of proximal and distal tubules will be examined. The result may vary with the site of blockage. Stop-flow pressures will also be measured in rats on a high or low salt diet. These results may suggest the participation of the renin-angiotensin system in the feedback mechanism. Finally, single nephrons will be microdissected after prolonged (e.g. one week) obstruction, to see whether nephron atrophy is induced.